Magnesium & phosphorus

Hypomagnesemia

Lyte disturbances (↓K, ↓Ca, alkalosis), hypoparathyroidism, lethargy, muscle weakness. Severe: delirium, coma, neuromuscular hyperexcitability (hyperreflexia, tetany, seizures), cardiovascular (↑QRS, peaked T waves, later ↑PR, ↑QTc, U waves, VT/TdP), and accentuation of digoxin toxicity (Med Sci (Basel) 2019;7:56; ).

GI: ↓ intake (AUD); ↑ loss (diarrhea, pancreatitis, malabsorption, small-bowel resection, PPIs); cellular shift (refeeding).
Renal wasting: thiazides, loops, amphotericin B, aminoglycosides, foscarnet, tacrolimus/cyclosporine, cisplatin, digoxin, pentamidine; inherited (Gitelman); T2DM; EtOH.
FEMg >4% suggests renal wasting rather than GI loss.

Slow repletion holds better than a dump-and-run. Oral (slow) vs IV (fast — typical inpatient).
Unstable: MgSO4 1–2 g over 2–15 min, may repeat ×2. Stable: 1–2 g over 30–60 min. Favor IV if symptomatic; the dose if CrCl <30.
PO: MgCl2 4–8 tabs/day causes less diarrhea than Mg oxide 800–1,600 mg/day; always divide doses.
Renal wasting: a K-sparing diuretic or SGLT2i can cut Mg excretion.

Hypermagnesemia

Usually only symptomatic if Mg >4, and rarely pathologic without renal insufficiency (). Mild: nausea, flushing, headache, lethargy, drowsiness. Severe: neuromuscular depression (hyporeflexia is the first sign, then weakness, respiratory failure); cardiovascular (hypotension, bradycardia, ↑PR / ↑QRS / ↑QTc, complete heart block, arrest); hypocalcemia (hyperMg suppresses PTH).

Mechanism: Mg intake exceeds renal clearance.
Med overdose: Epsom salts, laxatives, Maalox, Mg enemas — avoid these in ESRD and in pre-eclampsia / eclampsia treatment.
Gastritis / PUD / colitis increase Mg absorption.
Misc: DKA, hypercatabolic states (TLS), lithium, adrenal insufficiency, milk-alkali, iatrogenic repletion.

Treat only if symptomatic. Calcium gluconate 1 g IV over 10 min (or a drip) to counteract respiratory depression and cardiac toxicity. IVF plus a loop to enhance renal excretion. If ESRD, HD for removal.

Hypophosphatemia

Symptoms typically if phos <1.0 mg/dL, especially if acute: ↓ intracellular ATP → global cellular dysfunction → muscle weakness, AMS / encephalopathy, paresthesia, seizures, CHF, respiratory depression, proximal myopathy, rhabdomyolysis, dysphagia / ileus, hemolysis, bone and dental demineralization (pain, hypercalciuria, rickets / osteomalacia) (; ; ).

Redistribution into cells: ↑insulin (DKA / HHS treatment, refeeding), acute respiratory alkalosis (↑pH → ↑glycolysis), hungry-bone syndrome (Ca and phos deposit in bone immediately after parathyroidectomy).
↓ GI absorption: poor PO, chronic diarrhea, ↓ vitamin D, antacids or phosphate binders (aluminum, Mg, sevelamer).
↑ renal excretion: ↑PTH (1° or 2° hyperPTH), Fanconi (myeloma, tenofovir), ↑FGF-23 (genetic / paraneoplastic), meds (acetazolamide, metolazone, IV iron — ), osmotic diuresis (glycosuria), CVVH (especially high-dose), post-kidney transplant (residual ↑FGF-23 and PTH).
FEPO4 >5% suggests renal wasting rather than GI loss or redistribution.

Fix the cause (often a medication).
Severe (<1 mg/dL, or 1–2 mg/dL at high risk of crashing — e.g. refeeding) or symptomatic: IV Na or K phosphate 30 mmol q6h with frequent levels (15, 30, or 45 mmol doses). Switch to PO once >1.5 mg/dL. Give half-dose in CKD / ESRD. Aggressive IV phosphate can precipitate calcium → hypocalcemia (tetany, seizures, arrhythmia, hypotension) and AKI.
Asymptomatic (<2 mg/dL, not high risk): Na or K phosphate 1 mmol/kg/day PO in 3–4 divided doses, max 80 mmol/day.
Neutra-Phos: 1 packet = 250 mg phos (8 mmol); 7.1 mEq K, 6.9 mEq Na — prefer if you need K or want less Na.
K-Phos Neutral: 1 tab = 250 mg phos (8 mmol); 1.1 mEq K, 13 mEq Na.
If poorly tolerated (diarrhea): scheduled skim milk, 8 oz = 8 mmol phosphate.

Acute hyperphosphatemia

For chronic hyperphosphatemia, see CKD. Acute high phos precipitates calcium → hypoCa (cramps, tetany, tingling, perioral numbness) and acute nephropathy.

Acute phosphate load: TLS, rhabdomyolysis, exogenous / phosphate-containing laxatives, fosphenytoin.
Acute extracellular shift: DKA, lactic acidosis, severe hyperglycemia.
AKI or CKD from decreased clearance, including acute phosphate nephropathy.
Increased tubular reabsorption: vitamin D toxicity.
Pseudohyperphosphatemia: hyperglobulinemia, hyperlipidemia, hyperbilirubinemia, hemolysis.

Normal saline (can worsen hypocalcemia), HD if needed.
Low-phos diet, binders (sevelamer). Avoid IV calcium if Ca × Phos >70.
Renal consult if refractory or profound.
When both K and phos are high after chemo, think TLS (also uric acid, LDH) — IVF, rasburicase if indicated, dialysis by AEIOU.